title: Selective impairment of endothelium-mediated vasodilation in liver transplant recipients with cyclosporin A-induced hypertension.
abstract: Arterial hypertension is commonly observed in orthotopic liver transplantation (OLT) recipients receiving cyclosporin A (CsA), but the precise pathogenetic mechanisms remain partially unknown. The aim of this study was to investigate endothelium-dependent and -independent dilation and adrenergic constriction of resistance vessels of OLT recipients treated with CsA. Vascular reactivity was examined in 22 OLT patients, 10 with and 12 without arterial hypertension, and in 10 control subjects by assessing the forearm blood flow response to the brachial artery infusion of increasing concentrations of methacholine chloride, sodium nitroprusside, and phenylephrine. In 10 OLT patients, the response to methacholine was also examined after acetylsalicylate. The ratio of serum nitrite and nitrate to serum creatinine was lower (P < .05) in OLT patients with hypertension than in nonhypertensive patients and controls. Basal forearm flow was similar in the three groups. Methacholine vasodilation was impaired in the hypertensive patients as shown by a lower maximum forearm vasodilator response and a shift in the dose response curve to methacholine to the right compared with the nonhypertensive OLT patients and the controls. The response to methacholine was not modified after salicylate. Forearm flow response to nitroprusside was similar in the three groups. No differences between the patients and the controls were found in the maximum forearm flow contraction in response to phenylephrine. An impairment in endothelium-dependent vasodilation could mediate arterial hypertension in OLT patients immunosuppressed with CsA.
authors.affiliation: Department of Gastroenterology of Clínica Puerta de Hierro, Madrid, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Albillos
authors.forename: G
authors.initials: G
authors.lastname: Cacho
authors.forename: C
authors.initials: C
authors.lastname: Barrios
authors.forename: M
authors.initials: M
authors.lastname: Alvarez-Mon
authors.forename: I
authors.initials: I
authors.lastname: Rossi
authors.forename: J
authors.initials: J
authors.lastname: Gómez-Arnau
authors.forename: M
authors.initials: M
authors.lastname: Pérez-Páramo
authors.forename: J L
authors.initials: JL
authors.lastname: Calleja
authors.forename: J
authors.initials: J
authors.lastname: Muñoz
authors.forename: M T
authors.initials: MT
authors.lastname: Torres
authors.forename: R
authors.initials: R
authors.lastname: Daza
authors.forename: V
authors.initials: V
authors.lastname: Cuervas-Mons
authors.forename: P
authors.initials: P
authors.lastname: Escartín
mesh_terms: D000328:Adult; D016572:Cyclosporine / Q000009:adverse effects*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology; D016031:Liver Transplantation / Q000502:physiology*; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D016210:Methacholine Chloride; D009599:Nitroprusside; D010656:Phenylephrine; D016572:Cyclosporine